Can You Have a Stroke in Your Sleep and Not Know It

The circadian pattern in CVAs is similar to that in cardiovascular events, with a elevation in the early on morning after the patient awakens.^{1 2 3 iv 5 six vii 8} The circadian pattern of TIAs has not been reported, but transient myocardial ischemic events have a circadian pattern similar to that of other cardiovascular events.^{9 10} TIAs are probable to take a circadian pattern similar to that of other CVAs. Other risk factors have not been shown to be statistically different for TIAs and minor stroke.^{11 12 thirteen} Although the pinnacle in CVA occurrence is most frequently reported to be in the morning after the patient awakens, 13% to 44% of all CVAs are reported to occur during sleep, with symptoms becoming evident once the patient awakens.^{ii 3 four 5 6 14}

Recently, snoring has been shown to be an independent chance gene for the occurrence of stroke during wakefulness and sleep.^{15 16 17 18 nineteen} A history of snoring increases the odds ratio for access to the hospital for stroke 3.2-fold.^xix Additionally, the severity of snoring has been plant to be significantly related to increased mortality for the next 6 months after hospitalization.^xix When a history of sleep apnea, excessive daytime sleepiness, and obesity are all present in improver to snoring, the odds ratio for stroke has been shown to increase to viii.0.¹⁷

This report presents two cases of patients presenting with either TIA or minor stroke immediately on awakening from sleep; in both patients severe OSA was found, and handling of the OSA by NCPAP eliminated any farther episodes.

Case Reports

Case 1

The patient is a 64-twelvemonth-former, v-ft, 1-in, 218-lb white adult female admitted to the medical inpatient unit of the hospital. On the night before her admission the patient awoke suddenly from slumber at approximately 4 am. According to family unit members and to the patient herself, she was unable to produce any voice communication, although she could communicate by other means. Based on this description, her symptoms were idea to exist consistent with a motor aphasia. On inflow at the emergency section an hour later on, the patient's spoken language had improved and was described as "thick," characterized past significant hesitancy with difficulty in making transitions from sound to sound and very simplified vocabulary. Inside ane hour speech fluency had completely returned to normal with no apparent residual difficulties. She was additionally noted past emergency department physicians to be mildly empty-headed and lethargic at admission, although she was responsive and cooperative. These symptoms persisted for an additional hour after normal speech returned. Neurological examination was unremarkable except for the dysphasia. Blood pressure was 154/82 mm Hg. A CT of the head, carotid and transcranial Doppler sonograms, and an MRI angiogram of the carotid arteries were unremarkable. An echocardiogram showed left ventricular hypertrophy. The patient does not fume or utilize alcohol. She reported her usual sleep period as 12:30 am to 8 am. The patient's medical history was unremarkable, and she was taking no medications. Her laboratory studies were unremarkable except for borderline glucose intolerance, with claret glucose levels of 119 to 132 mg/dL. Arterial blood gases were measured several times during her hospitalization and were found to be within normal limits. Pulmonary function tests were besides within normal limits.

During her hospitalization the patient was noted to be somnolent, especially in the morning, and was noted by staff and doctors to snore loudly. All-nighttime pulse oximetry was ordered and showed continuous, repetitive, and cursory periods of O_two desaturation of 5% to l% throughout the night, with four periods approximately 90 to 120 minutes apart in which O₂ saturation savage well below l% (Fig 1). These periods of O_two desaturation were associated with a clear bradycardia-tachycardia blueprint in the electrocardiographic charge per unit, with changes of thirty to 50 beats per minute occurring oftentimes. This pattern was read equally consequent with severe OSA. Because of family problems the patient was discharged from the hospital confronting medical advice with an NCPAP machine empirically fix at a pressure of ten cm H₂O. She afterwards returned equally an outpatient to the Sleep Disorders Center laboratory for full polysomnography. This confirmed the presence of severe OSAS, and the periods of O₂ desaturation below 50% were shown to take occurred during definite REM sleep (summary information are presented in the Table). The patient returned the next dark for an NCPAP titration trial. Assistants of NCPAP at a pressure of 7.five cm H₂O reduced the RDI to 3.vii/h of sleep, which was inside normal limits. Sao ₂ did not decline below 87% even during REM slumber. The overall quality of slumber also showed substantial improvement, with deep sleep and REM sleep rebound present. During the subsequent 12 months since the showtime of treatment there has been no recurrence of TIAs and the patient has reported sleeping well, with increased daytime alertness.

Example 2

The patient is a 59-yr-former, five-ft, six-in, 260-lb blackness woman who presented to the Sleep Disorders Center every bit an outpatient with complaints of severe morning headaches and excessive daytime sleepiness. Additionally, she noted that approximately 6 months ago she had awakened from sleep with mild just noticeable numbness of the right side of her face and weakness in her right arm and hand and to a lesser degree in her right leg. She was able to move her limbs merely had minor impairment in motor ability and dexterity on the correct compared with the left side. These symptoms have improved in the last iv months, although she still complains of mild numbness and weakness during her waking hours. However, no objective neurological deficits were plant on examination at this time. Once or twice weekly she reports that the numbness and weakness are more than severe on enkindling from sleep in the morning but return to milder levels inside 1 to 6 hours. She besides complained of loud snoring and had awakened herself briefly with snores at least twice nightly. Additionally, she awakened two to three times for up to thirty minutes each time with sensations of gasping for breath associated with palpitations and occasionally with night sweats. During the last twelvemonth the patient has become increasingly sleepy during the mean solar day, falling asleep unintentionally whenever inactive. Twice she fell asleep briefly while driving.

The patient reported that these symptoms occurred equally a effect of a 30-lb weight gain during the final year. The patient related that the weight gain had occurred as a upshot of anxiety and low afterwards the sudden and unexplained death of her son. Her son (historic period, 39 years; pinnacle, half dozen ft, six in; weight, ≥350 lb) had been institute dead on his bed in the morning, fully clothed, with the television on. Ii postmortem examinations had failed to determine the cause of the death. On further questioning, the patient stated that her son had near all of the symptoms she herself had reported to usa. He was known every bit a loud snorer, noted by family members to awaken gasping for breath from sleep, and was extremely sleepy, prone to fall comatose all of a sudden whenever inactive. Based on his torso habitus and history provided by his family unit, it seemed highly likely that her son had suffered from untreated OSAS. Untreated moderate-to-severe OSAS is known to result in a statistically higher rate of mortality than in treated patients.²⁰

The patient'due south neurological examination, CT of the head, electrocardiogram, and carotid Doppler sonogram were unremarkable except for weakness noted in a higher place. She was hypertensive and had been treated for the terminal five years (currently with enalaprilat 20 mg, diltiazem threescore mg bid, and furosemide 40 mg). She took no other medications. Her medical history was remarkable for complaints of breast pain and palpitations for the last ii years and edema of the correct talocrural joint and leg. Arterial blood gases had non been examined recently. All the same, waking Sao _ii was 95% to 97% with the patient in the supine position.

Because of her own symptoms and her family history, the patient returned to the sleep laboratory for a diagnostic polysomnogram (Table and Fig two). It was consequent with severe OSA, with falls in Sao _ii well below l% during REM sleep only. The overall pattern was unusual in that although sleep-disordered breathing was present in non-REM sleep, it was of mild to moderate severity with minimal O₂ desaturation, while in REM sleep it was extremely astringent. Additionally, the patient reported that she had slept better in the sleep laboratory than she typically does at domicile. She awakened without the symptoms of weakness/numbness or headache. This was reflected in the better-than-expected quality of sleep. Many of the apneas and hypopneas produced only small-scale arousals, allowing the patient to accumulate good quantities of deep slumber. Considering sleep stages three and iv (deep slumber) are reported to suppress the advent of sleep apnea, this strongly suggested to us that during a "normal" night of slumber, apneas and hypopneas would occur more than frequently.²¹ The patient later returned for a handling trial of NCPAP during which administration of a pressure of 10.0 cm H₂O resulted in reduction in the RDI to iv.5/h of sleep, which was inside normal limits. Sao ₂ did not decline below 86% during REM sleep. A home NCPAP unit was prescribed, and in 6 months of home use the patient has reported only depression levels of numbness and weakness on awakening. Headaches and other symptoms accept been eliminated.

Discussion

Both patients awoke from sleep with signs and symptoms of TIA or minor stroke. Both patients were shown to take astringent OSAS with highly meaning periods of O_two desaturation, particularly in REM sleep. With successful treatment of OSA with NCPAP, there has been no recurrence of TIAs in the first patient or exacerbation of symptoms in the 2d patient.

A direct causal human relationship between sleep apnea and cerebrovascular symptoms cannot unequivocally be established because we did non direct detect the onset of cerebrovascular symptoms during sleep. Rather, they were reported to exist present immediately on awakening. However, a review of the literature constitute a unmarried, brief case report in abstruse grade of symptoms of TIA that appeared immediately after witnessed OSA and were confirmed by polysomnography.²² This study suggests that snoring and sleep apnea may not only be risk factors for TIAs just may sometimes be the firsthand trigger. This relationship is farther supported by the fact that administration of NCPAP in these two cases apparently prevented the recurrence of further symptoms.

OSAS is associated with many of the risk factors hypothesized to exist related to TIA and stroke. Reviews have reported that 48% to 96% of patients with diagnosed OSAS are hypertensive, and the severity of slumber apnea has been noted to be highly positively correlated with waking blood pressure, increases in intracranial pressure, decreases in cerebral perfusion pressure level with resultant changes in cognitive blood flow, and cardiac arrhythmias.^{23 24 25 26 27 28 29 30} Balfors and Franklin²⁹ recently reported that changes in cerebral blood flow and perfusion are then significant and rapid in patients with sleep apnea that cerebral autoregulation is insufficient to protect the brain from changes in arterial blood pressure. They suggest that along with apnea/hypopnea–induced hypoxemia, these changes in cerebral blood flow parameters predispose patients with sleep apnea to nocturnal cerebral ischemia.

Significant hypoxemia was associated with apneas and hypopneas that occurred primarily during REM sleep in both patients. The severity of these periods of O_two desaturation may take been exacerbated past the patients' obesity. Obesity has been shown to result in low lung volumes, particularly in the supine position, and has been reported to be significantly correlated with the caste of hypoxemia.^{31 32} REM sleep may have further exacerbated the hypoxemia as a result of longer durations of apnea/hypopnea noted during REM sleep in these patients and changes in lung mechanics acquired by loss of intercostal muscle activity and reduction in diaphragmatic tonic activity.^{31 32 33} Others accept suggested that REM sleep–related hypoxemia is due to relative hypoventilation compared with non-REM sleep.^{31 32 33} Upper airway closing pressures are besides reported to be lower in REM sleep compared with non-REM sleep, which suggests that airway plummet may occur more hands in REM sleep.³⁴ Obesity, alcohol, and age are also known risk factors of CVAs.^{17 35 36} OSAS is highly correlated with obesity, and alcohol is known to significantly exacerbate the severity of sleep apnea by increasing apnea duration and consequently O₂ desaturation.^{37 38 39 40}

OSAS is an easily diagnosed condition that should always be part of the differential diagnosis when TIAs or strokes occur during sleep. Not only is OSAS a take chances gene for the occurrence of CVAs, only because of its episodic and repetitive nature it could be the proximal trigger of TIAs and other CVAs. Successful treatment of patients with OSAS has been shown to reduce morbidity and mortality due to cardiovascular causes.^{41 42} Although long-term clinical and epidemiological data are lacking, our diagnosis and successful handling of two patients with TIA and pocket-size stroke during sleep by NCPAP suggests that patients with sleep-related CVAs should be evaluated for the presence of OSAS and treated if advisable. Since the occurrence of TIAs greatly increases the run a risk for future stroke, eliminating a risk gene such as slumber apnea might be considered primary prevention of stroke.^{eleven 12} Only long-term follow-up will show how constructive the diagnosis and handling of OSAS is as a preventive measure for TIAs and other CVAs.

Selected Abbreviations and Acronyms

CVA	=	cerebrovascular accident
NCPAP	=	nasal continuous positive airway pressure
OSA	=	obstructive sleep apnea
OSAS	=	obstructive sleep apnea syndrome
RDI	=	respiratory disturbance index
REM	=	rapid center motion
Sao 2	=	saturation with oxygen, arterial blood
TIA	=	transient ischemic attack

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Figure 1. All-night pulse oximetry screening done during hospitalization of patient 1. Console A shows frequent O₂ desaturation, with ii periods of astringent O₂ desaturation during which values declined below 50%. Panel B shows a repetitive bradycardia-tachycardia pattern in the electrocardiographic rate. These data were interpreted as consequent with severe OSA.

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Figure 2. Histograms of all-night sleep recording in the Sleep Disorders Eye for patient ii. Panel A shows surprisingly skilful-quality sleep. Panel B shows apneas and hypopneas, with nigh all obstructive (Obs.) apneas actualization during REM slumber. Panel C shows that the patient slept in the right lateral decubitus position. Panel D shows minimal O₂ desaturation during non-REM slumber and severe O₂ desaturation below l% during REM sleep.

Table 1. Diagnostic Polysomnogram and NCPAP Treatment Trial Information for Both Patients

	Patient 1		Patient two
	Polysomnogram	NCPAPT	Polysomnogram	NCPAPT
RDI	83.4/h	3.7/h1	22.0/h	4.5/h1
RDI in REM slumber	76.2/h	…	44.ii/h	…
Apneas+hypopneas, full no.	538	…	152	…
Obstructive apneas	51	…	63	…
Obstructive hypopneas	487	…	89	…
Mixed apneas	0	…	0	…
Central apneas	0	…	0	…
Lowest Sao 2, %	<l	89	<50	86ane
Longest apnea elapsing, southward	59	25	95	221
Optimal NCPAP, cm H2O	…	7.five	…	10.0
Total recording time, min	463.5	483.0	467.0	472.5
Total slumber time, min	387.0	361.0	414.5	379.0
Sleep efficiency, %	83.5	74.vii	88.viii	80.2
Stage i, min	87.5	33.5	20.0	34.5
Stage ane, %	22.six	9.3	four.eight	9.1
Phase 2, min	267.5	167.0	227.0	203.5
Stage 2, %	69.1	46.iii	54.8	53.7
Stages three+four, min	0.5	96.0	82.0	78.0
Stages 3+4, %	0.ane	26.6	19.viii	20.6
REM, min	31.5	64.5	85.5	63.0
REM, %	eight.1	17.9	twenty.6	16.6

This report was supported in part by the Lankenau Medical Research Eye.

Footnotes

Correspondence to Mark R. Pressman, PhD, Sleep Disorders Eye, The Lankenau Hospital and Medical Research Eye, 100 Lancaster Ave, Wynnewood, PA 19096-3498.

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Source: https://www.ahajournals.org/doi/10.1161/01.STR.26.12.2361

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